JaLCDOI 10.18926/AMO/47260
FullText URL 65_6_353.pdf
Author Ichihara, Eiki| Kiura, Katsuyuki| Tanimoto, Mitsune|
Abstract Angiogenesis is an essential process in tumor growth. The concept of angiogenesis, when proposed by Folksman in 1971, had a great impact on cancer research and therapy, as the survival and proliferation of cancer depend on angiogenesis, which could be a target of cancer therapy. In subsequent decades, numerous antiangiogenic agents were developed, and some of them have been applied clinically. However, angiogenesis includes a complex and multistep process that has not been sufficiently elucidated. In this review, we focus on signaling pathways related with tumor angiogenesis and several antiangiogenic agents approved by the United States Food and Drug Administration or under investigation.
Keywords angiogenesis cancer
Amo Type Review
Published Date 2011-12
Publication Title Acta Medica Okayama
Volume volume65
Issue issue6
Publisher Okayama University Medical School
Start Page 353
End Page 362
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2011 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22189475
Web of Sience KeyUT 000298516900001
Author Takeda, Hiromasa| Takigawa, Nagio| Ohashi, Kadoaki| Minami, Daisuke| Kataoka, Itaru| Ichihara, Eiki| Ochi, Nobuaki| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2013-02-15
Publication Title Experimental Cell Research
Volume volume319
Issue issue4
Content Type Journal Article
Author Ninomiya, Takashi| Takigawa, Nagio| Ichihara, Eiki| Ochi, Nobuaki| Murakami, Toshi| Honda, Yoshihiro| Kubo, Toshio| Minami, Daisuke| Kudo, Kenichiro| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2013-05
Publication Title Molecular Cancer Therapeutics
Volume volume12
Issue issue5
Content Type Journal Article
Author Hayakawa, Hiromi| Ichihara, Eiki| Ohashi, Kadoaki| Ninomiya, Takashi| Yasugi, Masayuki| Takata, Saburo| Sakai, Katsuya| Matsumoto, Kunio| Takigawa, Nagio| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2013-11
Publication Title Cancer Science
Volume volume104
Issue issue11
Content Type Journal Article
Author Murakami, Toshi| Takigawa, Nagio| Ninomiya, Takashi| Ochi, Nobuaki| Yasugi, Masaaki| Honda, Yoshihiro| Kubo, Toshio| Ichihara, Eiki| Hotta, Katsuyuki| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2014-01
Publication Title Lung Cancer
Volume volume83
Issue issue1
Content Type Journal Article
Author Ochi, Nobuaki| Takigawa, Nagio| Harada, Daijiro| Yasugi, Masayuki| Ichihara, Eiki| Hotta, Katsuyuki| Tabata, Masahiro| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2014-03-10
Publication Title Experimental Cell Research
Volume volume322
Issue issue1
Content Type Journal Article
Author Yasugi, Masayuki| Takigawa, Nagio| Ochi, Nobuaki| Ohashi, Kadoaki| Harada, Daijiro| Ninomiya, Takashi| Murakami, Toshi| Honda, Yoshihiro| Ichihara, Eiki| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2014-08-15
Publication Title Experimental Cell Research
Volume volume326
Issue issue2
Content Type Journal Article
JaLCDOI 10.18926/AMO/55587
FullText URL 71_6_505.pdf
Author Honda, Yoshihiro| Takigawa, Nagio| Ichihara, Eiki| Ninomiya, Takashi| Kubo, Toshio| Ochi, Nobuaki| Yasugi, Masayuki| Murakami, Toshi| Yamane, Hiromichi| Tanimoto, Mitsune| Kiura, Katsuyuki|
Abstract (−)-Epigallocatechin-3-gallate (EGCG) has been shown to bind to several receptors including epidermal growth factor receptor (EGFR). EGFR tyrosine kinase inhibitors and anaplastic lymphoma kinase (ALK) inhibitors are effective for non-small cell lung cancers harboring activating EGFR mutations and ALK or c-ros oncogene 1 (ROS1) fusion genes, respectively. We investigated the effects of EGCG on EGFR- or fusion gene-driven lung cancer cells such as PC-9, RPC-9, H1975, H2228 and HCC78. The five cell lines had similar sensitivity to EGCG. Phosphorylated (p)EGFR, pAkt and pErk in PC-9, RPC-9 and H1975 cells were suppressed by EGCG (50 or 100 μM). EGCG also inhibited pALK in H2228, pROS1 in HCC78, and pErk and pAkt in both cell lines. All the xenograft tumors established using the 5 cell lines in EGCG-treated groups were significantly smaller than the tumors in the vehicle-treated groups. The numbers of tumor blood vessels of xenograft tissues in EGCG-treated mice were significantly lower than those in vehicle-treated mice. In conclusion, EGCG may be effective for EGFR-driven lung tumors irrespective of the presence of T790M, and for ALK or ROS1 fusion gene-driven lung tumors.
Keywords epigallocatechin-3-gallate lung cancer EGFR ALK ROS1
Amo Type Original Article
Published Date 2017-12
Publication Title Acta Medica Okayama
Volume volume71
Issue issue6
Publisher Okayama University Medical School
Start Page 505
End Page 512
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2017 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 29276223
JaLCDOI 10.18926/AMO/56080
FullText URL 72_3_319.pdf
Author Makimoto, Go| Ichihara, Eiki| Hotta, Katsuyuki| Ninomiya, Kiichiro| Oze, Isao| Minami, Daisuke| Ninomiya, Takashi| Kubo, Toshio| Ohashi, Kadoaki| Tabata, Masahiro| Maeda, Yoshinobu| Kiura, Katsuyuki|
Abstract Although cisplatin-based chemotherapy shows a survival advantage compared to carboplatin for treating advanced non-small cell lung cancer, high-volume hydration and a long infusion time are necessary to avoid nephrotoxicity, and cisplatin-based chemotherapy has been difficult to administer in outpatient settings. A low-volume hydration method using mannitol or furosemide as forced diuresis was recently introduced, but there are no clear conclusions regarding which agent should be used. We describe our ongoing randomized phase II trial (the OLCSG1406 Study) evaluating the efficacy of forced diuresis. This study will clarify whether mannitol or furosemide is more suitable in cisplatin-based chemotherapy with low-volume hydration.
Keywords cisplatin mannitol furosemide lung cancer hydration non-small cell lung cancer
Amo Type Clinical Study Protocol
Published Date 2018-06
Publication Title Acta Medica Okayama
Volume volume72
Issue issue3
Publisher Okayama University Medical School
Start Page 319
End Page 323
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2018 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 29926012